Because Fas is the death receptor that mediates FasL-induced apoptosis, and it has been shown that FasL on CTLs plays an essential role in suppression of spontaneous tumor development18, 19, 43, it therefore seems that human colon carcinoma cells might use down-regulation of Fas as a mechanism to escape the host cancer immune surveillance to progress and metastasize. This evidence concerns the gene FAS and neoplasm.